Several growth related genes such as EGFR and VEGF as well as tumour suppressor genes such as p53 have been implicated in LC pathogenesis and progression.
The serum VEGF and TGF-β concentration in PPA group was significantly lower than that in SGA group (P < 0.05).Thoracic paravertebral nerve block-propofol intravenous general anesthesia can reduce the dosage of opioids, improve the effect of postoperative analgesia, and reduce the serum concentration of tumor angiogenesis-related factors in patients undergoing radical resection of lung cancer.
Through <i>in vitro</i> and <i>in vivo</i> experiments, we found that different doses of OMT could up-regulate miR-520, selectively inhibit VEGF and thus inhibit the proliferation and migration of lung cancer.
Vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) have been implicated in the invasion and metastasis of various malignant tumor types, such as lung cancer and gastric carcinoma.
We demonstrated that Nef protein reprograms initial stages of lung cancer (e.g. changes in the metabolism, improved cell survival and invasion, increase the angiogenesis factor VEGF).
The potential mechanism was inhibiting cell proliferation and inducing apoptosis in lung cancer by the regulation of vascular endothelial growth factor A expression.
The nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; nicotine derived nitrosamine ketone) is one of the strongest carcinogens in tobacco which is involved in induction of lung cancer by changing the stimulation of vascular endothelial growth factor (VEGF) and annexin A2 expression.
To investigate the antitumor effect of endostatin in lung cancer, the present study was designed to explore the alterations of microvessel density in Lewis lung cancer models and the expression of vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-17, interferon (IFN)-γ and hypoxia inducible factor (HIF)-1α, following endostatin therapy.
In vivo studies in lung cancer bearing mice have revealed the superior therapeutic activity of LbL-RAP-BER/SLS-NPs over the free drugs as demonstrated by 88.09% reduction in the average number of microscopic lung foci and 3.1-fold reduction of the angiogenic factor VEGF level compared to positive control.
To investigate the effects of dalteparin sodium on the expression of vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR), and hypoxia-inducible factor 1α (HIF-1α) in A549 human lung cancer (LC) cell line and a human A549-grafted nude mouse model.
In this article, we review the detection methods designed to measure the VEGF levels in different body fluids and prognosticate the value of VEGF in treatment, diagnosis and survival in lung cancer.
In conclusion, we identified the relationship between HIF-1α/VEGF pathway and response to radiotherapy and its role in angiogenesis in lung cancer in vitro.
The present study intended to investigate efficacy of radiotherapy in the treatment of intermediate and advanced stage lung cancer and the effects on serum vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9).
We made the following findings: (1) the human heart, muscle, eye, pancreas, and lymph node are among the tissues with the highest APs; (2) tissues with high APs have more active angiogenic pathways and angiogenic C/C responses; (3) inflammatory TRs dominate regulation of all angiogenic C/Cs; homeostatic TRs regulate all to a lower extent, while endothelial cell-specific TRs mainly regulate pro-angiogenic and bi-functional C/Cs; (4) tissue AP is positively correlated with the expression of oxygen sensors PHD2 and HIF1B, VEGF pathway gene VEGFB, and stem cell gene SOX2; (5) cancers of the digestive system tend to have increased angiogenesis dominated by endothelial cell-specific pro-angiogenic pathways, while lung cancer and prostate cancer have significantly decreased angiogenesis; and (6) endothelial cell-specific pro-angiogenic pathways are significantly increased in thrombus-derived leukocytes in patients with acute coronary artery disease.
In conclusion, the SNPs examined appear to influence lung cancer susceptibility while as genotypes of the SNPs don't appear to have significant association with VEGF mRNA expression in lung tumours.
Our results indicate that HPV16 E6/E7 indirectly upregulated the expression of vascular endothelial growth factor by inhibition of liver kinase B1 expression and upregulation of hypoxia-inducible factor 2α expression, thus propose a human papillomavirus-liver kinase B1-hypoxia-inducible factor 2α-vascular endothelial growth factor axis for the tumorigenesis of lung cancer.